Recent evidence, by both hemolytic complement and immunofluorescence assays, suggest that pemphigus and bullous pemphigoid are autoimmune skin diseases mediated by the complement system. In this respect, low levels of complement and individual components are present in blister fluids when compared to sera. An anticomplementary factor, now thought to represent an immune complex, has been identified in pemphigus blister fluid. Clq and C4 deposition occurs in skin lesions of both diseases in addition to C3. Properdin and C3 proactivator have also been implicated in both diseases and herpes gestationis. The immunopathology of this latter disease is still unclear. Further patients with these diseases will be studied for evidence of classical and alternate pathway activation of complement, biologic activities associated with the complement system, and immune complex formation.